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Journal Article

Modulation of HIV-1 Gag/Gag-Pol frameshifting by tRNA abundance.

MPS-Authors
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Korniy,  N.
Department of Physical Biochemistry, MPI for Biophysical Chemistry, Max Planck Society;

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Goyal,  A.
Department of Physical Biochemistry, MPI for Biophysical Chemistry, Max Planck Society;

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Samatova,  E. N.
Department of Physical Biochemistry, MPI for Biophysical Chemistry, Max Planck Society;

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Peske,  F.
Department of Physical Biochemistry, MPI for Biophysical Chemistry, Max Planck Society;

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Rodnina,  M. V.
Department of Physical Biochemistry, MPI for Biophysical Chemistry, Max Planck Society;

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Fulltext (public)

3047376.pdf
(Preprint), 5MB

Supplementary Material (public)

3047376_Suppl.pdf
(Supplementary material), 2MB

Citation

Korniy, N., Goyal, A., Hoffmann, M., Samatova, E. N., Peske, F., Pöhlmann, S., et al. (2019). Modulation of HIV-1 Gag/Gag-Pol frameshifting by tRNA abundance. Nucleic Acids Research, (in press). doi:10.1093/nar/gkz202.


Cite as: http://hdl.handle.net/21.11116/0000-0003-6008-8
Abstract
A hallmark of translation in human immunodeficiency virus type 1 (HIV-1) is a -1 programmed ribosome frameshifting event that produces the Gag-Pol fusion polyprotein. The constant Gag to Gag-Pol ratio is essential for the virion structure and infectivity. Here we show that the frameshifting efficiency is modulated by Leu-tRNALeu that reads the UUA codon at the mRNA slippery site. This tRNALeu isoacceptor is particularly rare in human cell lines derived from T-lymphocytes, the cells that are targeted by HIV-1. When UUA decoding is delayed, the frameshifting follows an alternative route, which maintains the Gag to Gag-Pol ratio constant. A second potential slippery site downstream of the first one is normally inefficient but can also support -1-frameshifting when altered by a compensatory resistance mutation in response to current antiviral drug therapy. Together these different regimes allow the virus to maintain a constant -1-frameshifting efficiency to ensure successful virus propagation.